Salbutamol-induced narrow QRS tachycardia: what is the mechanism?
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Biomedical subjects
Publications and source records attributed to Maria Pia Calabrò.
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We report a case of right bundle-branch block (RBBB) showing a QRS configuration typical for left bundle-branch block (LBBB) in leads V(5) and V(6). The QRS axis was at +90 degrees, and the QRS duration was 0.14 second. There were wide S waves in leads I and aVL, suggesting at first glance an RBBB, but the QRS morphology in the inferior leads (monophasic R wave with secondary ST-T changes) was more consistent with an LBBB. Lead V(1) suggested an RBBB, whereas leads V(5) and V(6) showed a monophasic R wave as in LBBB; moreover, a negative T wave, typical of LBBB, was present in lead V(5). Placement of the electrodes of leads V(4), V(5), and V(6) 2 intercostal spaces above restored in these leads a QRS configuration suggestive of RBBB. The diagnostic problem was mainly caused by the inferior direction of the QRS axis. Because the electrode of V(6) is normally placed below the electrical center of the heart, namely, on a plane that is not orthogonal to the sagittal plane, a vector directed mainly inferiorly and slightly to the right does not project on the negative part but on the positive of the lead line. For this reason, the S waves normally observed in the left precordial leads with RBBB disappear. The superior displacement of the electrodes "normalizes" the plane upon which the lead lines lie, thereby restoring the expected QRS configuration.
This presentation deals with a case of atrial flutter. During 2:1 A/V conduction, the QRS complexes showed a regular alternation of narrow beats and wide beats with a typical configuration of left bundle branch block. In contrast, pauses resulting from 4:1 A/V conduction ratio always resulted in narrow beats. Disappearance of left bundle branch block with long R-R intervals demonstrated that the block was tachycardia-dependent or phase 3. Analysis of the tracing suggested that narrowing of QRS complexes in alternate beats was due to supernormal left bundle branch conduction associated with retrograde concealed conduction into the anterogradely blocked bundle branch.
The aim of the present study was to evaluate the pulmonary sequelae and diaphragmatic motility in infant, adolescent and adult patients (pts) who had undergone the repair of a congenital diaphragmatic hernia. Thirty-one (81.5%) out of 38 survivors after left side CDH repair, without using a patch, were followed-up. They were subdivided in two groups. Group A (mid-term follow-up): 12 pts (39%) (5 males, 7 females) with a mean age of 4.5 years; Group B (long-term follow-up): 19 pts (61%) (9 males, 10 females) with a mean age of 21.0 years. All pts underwent physical examination, chest X-ray, diaphragmatic ultrasonographic (US) examination, pulmonary perfusion scintigraphy. Patients of the group B were also submitted to spirometry. All pts had a normal life-style and no one complained of respiratory symptoms. The chest X-ray revealed pathologic findings in 12 pts (39%). 8 pts (26%) showed chest wall alterations. The profile of the left diaphragmatic dome appeared irregular in 9 pts (29%). In all pts M-mode sonography disclosed a reduced diaphragmatic motility on the treated side. The mean pulmonary perfusion scintigraphy value on the affected side was 39.2+/-0.7%. The spirometric study showed normal values. We noted that the lung perfusion significantly and rapidly improved after CDH repair even the apparently hypoplastic and small lungs, the diaphragm maintained a good contractility during forced respiration.
BACKGROUND/PURPOSE: A few studies have taken into account the diaphragmatic function in patients successfully treated for congenital diaphragmatic hernia (CDH). Monodimensional sonography has been reported to be useful in assessing the diaphragmatic motility. Aim of the present study was to investigate, in a long-term follow-up, the diaphragmatic function after CDH repair. METHODS: Ten patients, with a mean age of 16 (5-26) years, were enrolled. All had had a left diaphragmatic hernia repaired, but no one received a patch. Ten subjects of matched age were used as controls. The diaphragmatic excursions appear, at M-mode sonography, as a sinusoid; the amplitude of the curve on the vertical axis measured the movement in centimeters. Chest x-ray and spirometry were also performed in CDH patients. RESULTS: A reduced diaphragmatic motility on the left (treated) side was recorded. The amplitude of the contraction was significantly reduced when compared with the contralateral side (1.19 +/- 0.2 vs 2.33 +/- 0.9 cm; P = .017) and was also significantly reduced in comparison with the motion of the left side of controls (1.19 +/- 0.2 vs 1.83 +/- 0.4 cm; P = .01). There was no difference in the amplitude of contraction between the left and right sides of control patients and between the right side of CDH patients and the controls. Spirometry was normal in all patients but one, who had a slight reduction of ventilation on the left side. CONCLUSION: M-mode sonography appears as a very useful tool in quantitative evaluation of diaphragmatic movements and should be extensively used during follow-up of patients after CDH repair. Motility of the repaired diaphragmatic is reduced, even after a long period, but this does not affect the respiratory function in patients who survived CDH repair.
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This article reports a case of tachycardia-dependent right bundle branch block (RBBB) occurring during atrial fibrillation. In some sections of the recording, an alternans occurs between complexes with a complete RBBB pattern and complexes showing normal intraventricular conduction or incomplete RBBB. Alternans is frequently observed during phases of fast and nearly regular rhythm, but it occurs even in the presence of a markedly irregular ventricular response. The RBBB alternans associated with short and regular RR intervals is likely to represent a manifestation of 2:1 bundle branch supernormal conduction, whereas alternans occurring with irregular cycles expresses a complex interaction between the RR cycle length and some mechanisms affecting intraventricular conduction, such as tachycardia-dependent bundle branch block, supernormal conduction and concealed retrograde activation of the anterogradely blocked bundle branch (the so-called "linking" phenomenon).
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